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PubMed1977

Some effects of dieldrin and mirex on Ehrlich ascites tumor cells in vivo and in vitro.

The effects of dieldrin and mirex on Ehrlich ascites tumor cells were assessed, using certain in vivo (in mice) and in vitro measurements. Mirex retarded the development of Ehrlich ascites tumor in vivo, but dieldrin did not. Effects of dieldrin on de nova RNA purine synthesis from formate in vivo were slight, while mirex inhibited the synthesis of both RNA purines. Dieldrin inhibited the in vitro incorporation if thymidine, uridine, and L-leucine into DNA, RNA, and protein, respectively, but mirex was virtually without effect.

Animals↗

PubMed1983

Effects of DDT and dieldrin on intestinal glucose transport and brush border hydrolases. A comparison with phenobarbital and methylcholanthrene.

The enhancement of in vitro small intestinal transcellular glucose transport in NMRI mice after oral administration of the organic pesticides 2,4-DDT and dieldrin can be shown to be due to an increased active transport at the site of the brush border membrane. Intestinal disaccharidase activities were concomitantly elevated in the dieldrin group, while DDT produced no effects with intestinal hydrolases. The classic enzyme inducing agents phenobarbital and methylcholanthrene failed to stimulate intestinal glucose transport, although both increased intestinal disaccharidase activities considerably, thus questioning a close relation between these digestive and absorptive functions in the translocation of glucose. Intestinal alkaline phospatase activity was enhanced after DDT, dieldrin and methylcholanthrene treatment, but not with phenobarbital. It is suggested that DDT and dieldrin exert their stimulating effect on intestinal glucose transport by a mechanism different from general induction of metabolic pathways.

Animals↗

PubMed1976

Enhancement of microsomal monooxygenase, epoxide hydrase and UDPglucuronyltransferase by aldrin, dieldrin and isosafrole administrations in rat liver.

The effects of intraperitoneal administration of aldrin (10 mg/kg), dieldrin (10 mg/kg) and isosafrole (50 mg/kg) were investigated on the activities of drug biotransformation enzymes in rat liver. All the compounds studied were found to enhance the activities of microsomal monooxygenase (e.g. p-nitroanisole O-demethylase, aryl hydrocarbon hydroxylase), epoxide hydrase (styrene oxide as substrate) and UDPglucuronyltransferase (p-nitrophenol as aglycone). Dieldrin, the epoxidized derivative aldrin, the eposidized derivative of aldrin, was a more potent inducer than the parent compound itself. NADPH CYTOCHROME C REDUCTASE ACTIVITY WAS EHANCED 2.5-FOLD, P-NITROANISOLE O-demethylase 7-fold, benzpyrene hydroxylase 2-fold, and epoxide hydrase 5-fold after treating rats with dieldrin for 6 days. The increase in activity of the microsomal UDPglucuronyltransferase could be only detected after an in vitro digitonin treatment of microsomal membranes, the enhancement being about 1.5-fold after administering dieldrin for 6 days. The administration of isosafrole to rats increased especially p-nitroanisole O-demethylase activity in liver microsomes (10-fold in 3 days). NADPH cytochrome c reducatase activkty was increased 2-fold, cytochrome P-450 content 1.2-fold, benzpyrene hydrozylase activity 2.5-fold and epoxide hydrase activity 1.2-fold after treatment of rats for 3 days. UDPglucuronyltransferase activity increased 2.2-fold by treating rats for 6 days with isosafrole. This increase was, however, only to be seen in in vitro digitonin-activated microsomes due to the latency of UDPglucuronyltransferase.

Aldrin↗

PubMed1986

Relevance of hyperglycemia to dieldrin toxicity in suckling and adult rats.

Acute exposure to dieldrin (HEOD) causes hyperglycemia and death in the adult rat. Whether the hyperglycemia contributes to the mortality was studied in 10- and 60-day-old Wistar rats given an LD50 dose of the insecticide (pups, 28 mg/kg p.o. and adults, 63 mg/kg p.o.). HEOD elevated blood glucose 2-fold in the adult but had no effect in the pup. d-Glucose (6 g/kg p.o., 0, 3, 6 and 18 h post HEOD) reduced by 79% the 24-h mortality the insecticide caused in the 10-day-old rat. Thus, hyperglycemia in the immature rat protects against dieldrin toxicity. Conversely, the 24-h mortality was not significantly affected in adult rats whose HEOD-induced hyperglycemia was increased with either d-glucose (6 g/kg p.o., every 2 h post HEOD) or 2-deoxyglucose (1 g/kg s.c., concomitant with the HEOD). Phenobarbital (40 mg/kg i.p., concomitant with the insecticide) significantly decreased both the hyperglycemia (23%) and the 24-h mortality (86%) in HEOD-treated adult rats. The administration of d-glucose (6 g/kg p.o., 0, 3, 9 and 18 h post HEOD) to phenobarbital and HEOD-treated animals restored the hyperglycemia and returned the 24-h mortality to that found in animals given dieldrin alone. Thus, in the adult rat HEOD-induced hyperglycemia is a component of dieldrin toxicity.

Administration, Oral↗

PubMed1987

Suppression of humoral immunity in inbred mice by dieldrin.

The effect of single, sublethal i.p. injection of dieldrin on the primary antibody response to thymodependent (sheep red blood cells, SRBC) and T-cell-independent (lipopolysaccharide, LPS) antigens were investigated in inbred C57Bl/6 mice. Time-course studies showed significant suppression of the anti-SRBC IgM and anti-LPS IgM response at 7-24 days and at 4-14 days, respectively, after exposure to 0.6 LD50 of dieldrin. The anti-SRBC IgG response was also suppressed by dieldrin exposure, however, maximal suppressory effect was found at 48 days after the pesticide exposure. Similar patterns of the dieldrin-induced suppression of the primary IgM response to the thymodependent and T-cell-independent antigens, in addition to the overall control of cytotoxicity of lymphoid cell populations, suggest rather dysfunction of cellular cooperation during the inductory phase of the immune humoral response.

Animals↗

PubMedDate not supplied

Interactions between endosulfan and dieldrin on estrogen-mediated processes in vitro and in vivo.

There is growing concern that estrogenic chemicals, both natural and human-made, may be causing a variety of reproductive disorders in wildlife and human populations. Recent in vitro data suggest that the interaction between some weakly estrogenic organochlorines, dieldrin, endosulfan, toxaphene, and chlordane, causes a synergistic increase in their estrogenic potency, an effect due to joint action on estrogen receptors (ER). As these studies were conducted using models of estrogen action derived from cells that are not physiologically controlled by estrogens, the relevance of these findings to human health are not clear. The present studies were conducted to examine the interaction between endosulfan and dieldrin in the activation of ER in or extracted from mammalian cells. Endosulfan and dieldrin showed no synergism in displacing 3H-E2 from rat uterine ER or in inducing the proliferation of MCF-7 breast cancer cells, an estrogen-dependent response. Furthermore, endosulfan (0.1 mg per animal per d) or dieldrin (0.1 mg), alone or in combination, injected intraperitoneally daily for 3 d, did not stimulate any uterotrophic activity nor had any effect on pituitary prolactin or other endocrine-related endpoints in immature female rats. These studies demonstrate that these weakly estrogenic compounds do not interact in a synergistic fashion in binding to ER or in activating ER-dependent responses in mammalian tissues or cells. Thus, these results suggest that coexposure to these weakly estrogenic environmental contaminants likely will not cause human reproductive toxicity related to estrogen action.

Animals↗

PubMed2001

Comparison of base-excision repair capacity in proliferating and differentiated PC 12 cells following acute challenge with dieldrin.

Dieldrin, an organochlorine pesticide and known neurotoxicant, is ubiquitously distributed in the environment. Dieldrin depletes brain monoamines in some animal species and is toxic for dopaminergic neurons in vitro. Dieldrin interferes with mitochondrial electron transport and increases generation of superoxide anion. Reactive oxygen species have been shown to produce oxidative lesions to DNA bases, i.e., 8-hydroxy-2'-deoxyguanosine (8-oxodGuo). Accumulation of 8-oxodGuo has been shown to be promutagenic in proliferating cells, and can lead to degeneration in fully differentiated cells. The objective of this study was to determine the effects of dieldrin exposure on the activity of the enzyme responsible for removing 8-oxodGuo, OGG1, from undifferentiated (untreated with NGF) and differentiated (NGF-treated) PC 12 cells. Proliferating PC 12 cells exhibited a mild upregulation of glycosylase activity, reaching a maximum by 1 h and returning to baseline by 6 h. Differentiated (+) NGF cells showed a time-dependent decline in activity reaching a nadir at 3 h with a return towards baseline by 6 h. Levels of the damaged base, 8-oxodGuo, in the differentiated PC12 cells appeared to be regulated by the activity of OGG1. In contrast, levels of the damaged base in actively proliferating cells were independent of the OGG1 activity. This difference between actively dividing and differentiated cells in the regulation of base-excision repair and DNA damage accumulation explains, in part, the vulnerability of postmitotic neurons to oxidative stresses and neurotoxins.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed2000

Dieldrin resistance in Lucilia cuprina (the australian sheep blowfly): chance, selection and response.

Discrete-generation population cages of Lucilia cuprina were initiated with dieldrin-resistant allele (Rdl ) frequencies of 1 or 5% and maintained for 17 generations on media with concentrations of dieldrin in the range 0-0.006% (w/v). The probability of the initial establishment of the Rdl allele in a population was consistently greater at the 5% frequency and dependent on the concentration of dieldrin in the medium for both starting frequencies. Once the resistant allele was established responses to selection were concentration-dependent. It was concluded that in the absence of dieldrin the susceptible allele was selectively favoured, at 0. 00005% (w/v) concentration selection and random genetic drift influenced changes in allele frequency and at concentrations above this the Rdl allele was at a selective advantage. Fixation of Rdl occurred at the higher concentrations. The influence of random genetic drift and selection on the genetic response during the evolution of insecticide resistance is discussed.

Alleles↗

PubMed1984

Dieldrin and diazinon resistance in populations of the Australian sheep blowfly, Lucilia cuprina, from sheep-grazing areas and rubbish tips.

Populations of L. cuprina collected from adjacent sheep-grazing areas and rubbish tips in Victoria (Mansfield and Warrnambool) and New South Wales (Lismore) were tested for resistance to the insecticides diazinon and dieldrin. Populations from sheep-grazing areas had a significantly higher diazinon Rop-1 allele frequency than those from adjacent tips with the Victorian populations being more resistant than those from Lismore. Victorian sheep and tip populations had similar gene frequencies at the dieldrin resistance locus, but the Rdl allele frequency was significantly greater in the population at the tip than in the population from the sheep-grazing area at Lismore. The Rdl allele is at a higher frequency in flies from the Lismore area than in Victorian populations. The results at both loci are explained by a balance of selection and gene flow between sheep and tip populations and by selective differences between geographical areas. The exceptionally high frequency of the dieldrin Rdl allele in populations at the Lismore tip may be partially explained by the use of dichlorvos for fly control. Dosage mortality curve and genetic analyses suggest that dichlorvos (an organophosphorus compound) may select at the dieldrin resistance locus. Possible mechanisms for this are discussed. The consequences of genetic differentiation between L. cuprina populations within a region for an autocidal control program are considered.

Animals↗

PubMed1979

Effects of dieldrin on operant behavior of bobwhites.

Bobwhites (Colinus virginianus) were trained to peck a green lighted key to receive food. Bird response performance was monitored for 14 days, then birds were dosed with five levels of dieldrin (50 to 300 micrograms every other day) for 42 days while their response performance was monitored. At the end of the 42-day dosage period, mean brain concentrations of dieldrin ranged from 2.6 ppm to 11.8 ppm; lower concentrations associated with lower dosage levels. All dieldrin dosage levels altered cage behavior of bobwhites, dieldrin dosage levels greater than 100 micrograms resulted in slower and less accurate responses by dosed birds during the 42-day trial period.

Animals↗

PubMed2002

Toxicity, bioaccumulation and tissue partitioning of dieldrin by the shrimp, Macrobrachium faustinum de Sassure, in fresh and brackish waters of Jamaica.

The 2-week no observed effect (NOEC) and lowest observed effect (LOEC) concentrations of dieldrin were determined for Macrobrachium faustinum de Sassure in fresh and brackish waters. LOEC1,10,50,95 values in fresh water were 0.001, 0.003, 0.011 and 0.058 microg l(-1), respectively, and in brackish water, 0.00006, 0.00027, 0.00165, and 0.0172 microg l(-1), respectively. The 96-hr LC10, LC50 and LC95 values were 0.029, 0.123 and 0.771 microg l(-1), respectively. It is proposed that NOEC and LOEC be redefined to take into account the percentage of individuals affected, the severity of symptoms and the recovery of poisoned individuals. Two new terms are proposed--Median Observable Effect Concentration (MOEC) for pronounced toxic symptoms in most individuals but mortality in <50%, and Pronounced Observed Effect Concentration (POEC), which inflicts mortality in >50% individuals. Bioaccumulation of dieldrin by M. faustinum from surrounding fresh and brackish waters were rapid and fairly uniform for the first 48 h when the bioconcentration equilibrium (14.4 +/- 0.42 ng g(-1) at 0.001 microg l(-1) and 42.5 +/- 1.72 ng g(-1) at 0.01 phi g l(-1)) was achieved. Relative partitioning of residues (ng g(-1) wet wt.), after 24h exposure to 0.001 microg l(-1) of dieldrin in fresh water, in the different tissues was hepatopancreas > gonads > gills > large claws > muscle and exoskeleton. Shrimp which had accumulated 10.5 +/- 0.52 ng g(-1) dieldrin in fresh and brackish water, eliminated only about 52% of the residues after eight days in uncontaminated water.

Animals↗

PubMed1977

DDVP (dichlorvos) detoxification by binding and interactions with DDT, dieldrin, and malaoxon.

Binding to tissue carboxylesterases has been suggested as an important mechanism of detoxification for several organophosphates. In this study DDVP, malaoxon, and paraoxon were inactivated, in vitro, by mouse liver under assay conditions that were consistent with a binding mechanism of inactivation. Binding of the three organophosphates was inhibited in livers of mice pretreated, 18 hr before sacrifice, with TOTP (triorthotolyl phosphate, 125 mg/kg, ip). Previous studies have shown that similar TOTP treatment enhanced the toxicity of malaoxon and paraoxon but did not alter the toxicity of DDVP. Both DDT (50 mg/kg, ip, given 4, 3.5, and 2.5 days before sacrifice) and dieldrin (16 mg/kg, po, given 4 days before sacrifice) increased liver/body weight ratios and decreased the duration of pentobarbital-induced loss of righting ability. Dieldrin increased liver carboxylesterase activity and liver binding of malaoxon and paraoxon but not of DDVP. In contrast, DDT did not increase liver carboxylesterase activity nor did it increase binding of malaoxon or paraoxon. Yet DDT pretreatment increased mouse liver binding of DDVP. Neither DDT nor dieldrin pretreatments altered the toxicity of subsequently administered DDVP. These results support the hypothesis that carboxylesterase binding does not represent an important mechanism for DDVP detoxification in the mouse. In other experiments, in vitro inactivation of malaoxon by binding was inhibited in livers of mice given DDVP (30 mg/kg, ip) 30 min before sacrifice. Similar DDVP pretreatment potentiated the anticholinesterase action of malaoxon (10 mg/kg, ip). Thus, even though DDVP toxicity was not altered by DDT- or dieldrin-induced changes in organophosphate binding, DDVP inhibited malaoxon binding and increased malaoxon toxicity.

Animals↗

PubMed1988

Effect of subchronic dieldrin treatment on calmodulin-regulated Ca2+ pump activity in rat brain.

Calmodulin-dependent (CaM-dependent) and nondependent Ca2+ pump activity was determined in the brain P2 fraction of Sprague-Dawley rats treated in vivo with 10 ppm dieldrin for 60 d. After 40 d of dieldrin intoxication, daily food consumption and body weight gain were found to be affected. Dieldrin inhibited both CaM-dependent and -independent Ca2+-ATPase activity and the enzyme activity decreased to 36% (CaM-dependent)--and 18% (basal) respectively after 60 d of intoxication. Reduction in brain CaM levels and a subsequent inhibition of Ca2+-ATPase activity suggests that chronic intoxication of dieldrin at very low doses alters calmodulin and its regulation of Ca2+-ATPase activity.

Animals↗

PubMed1992

The tumour promoters dieldrin and phenobarbital increase the frequency of c-Ha-ras wild-type, but not of c-Ha-ras mutated focal liver lesions in male C3H/He mice.

The frequency and pattern of mutations at codon 61 of the c-Ha-ras protooncogene were analysed in glucose-6-phosphatase-deficient hepatic lesions of male C3H/He mice occurring either spontaneously or after continuous treatment with 10 p.p.m. dieldrin or 500 p.p.m. phenobarbital (PB) in their diet. At 52 weeks after start of promoter administration, enzyme-altered liver lesions had developed in 41% (15/37) of untreated control mice and in 67% (10/15) and 63% (10/16) of mice treated with dieldrin or PB respectively. The average numbers of focal lesions per mouse were 0.57 in the control, 1.5 in the dieldrin and 1.0 in the PB group. Lesions were punched out from frozen liver sections and used for mutation analysis by allele-specific oligonucleotide hybridization following in vitro amplification of DNA via polymerase chain reaction. In the control group, 12 out of 21 liver lesions (57%) showed c-Ha-ras mutations, while five out of 23 (22%) and four out of 16 (25%) lesions were mutated in the dieldrin and PB groups. Taking the different numbers of animals in the three experimental groups into account, our data indicate that the tumour promoters increased the frequency of c-Ha-ras wild-type but not of c-Ha-ras mutated focal liver lesions, suggesting that the mutations had occurred spontaneously and were not related to treatment. Since c-Ha-ras mutations were found to be frequent in large but infrequent in small hepatocellular lesions, these mutations may represent in livers of C3H/He mice an endogenous promoting principle that provides a selective growth advantage to the mutated progenitor cells.

Amino Acid Sequence↗

PubMed1981

National study of chlorinated hydrocarbon insecticide residues in human milk, USA. I. Geographic distribution of dieldrin, heptachlor, heptachlor epoxide, chlordane, oxychlordane, and mirex.

Human milk samples obtained from 1436 women residing in the United States were analyzed by gas-liquid chromatography for the chlorinated hydrocarbon insecticides--dieldrin, chlordane, heptachlor, heptachlor epoxide, oxychlordane and Mirex. Dieldrin was found above the detection limit (1.0 ppb) in over 80% of all the samples collected. Chlordane was not found in any of the 1436 milk samples but its metabolite, oxychlordane, was found above the detection limit in 74% of the samples. Although heptachlor was recovered in less than 2% of the samples, its metabolite, heptachlor epoxide, was found above the detection limit in 63% of the samples. It was of considerable interest that Mirex was not positively identified in any of the samples. The proportion of samples with values above the detection limit for dieldrin, heptachlor epoxide and oxychlordane varied significantly among the five geographic regions with the southeastern United States having the highest mean residue level for each of these three contaminants. For the United States the mean fat adjusted residue levels of those samples above the detection limit were 164.2 ppb for dieldrin, 91.4 ppb for heptachlor epoxide, and 95.8 ppb for oxychlordane.

Adult↗

PubMed2005

Independent mutations in the Rdl locus confer dieldrin resistance to Anopheles gambiae and An. arabiensis.

Substitutions of a conserved alanine residue in the Rdl locus coding for a gamma-aminobutyric acid (GABA) receptor subunit with serine or glycine confer resistance to dieldrin in various insect species. Here, we show that alanine to glycine substitution in the Rdl locus of the malaria vector, Anopheles gambiae, is genetically linked to resistance to dieldrin. An alanine to serine substitution developed independently in a dieldrin resistant strain of An. arabiensis. An allele-specific polymerase chain reaction (PCR) assay was able to differentiate dieldrin resistant and susceptible mosquitoes.

Amino Acid Sequence↗

PubMed1995

Actions of the insecticide fipronil, on dieldrin-sensitive and- resistant GABA receptors of Drosophila melanogaster.

1. Blocking actions of the novel insecticide, fipronil, were examined on GABA responses recorded from Xenopus oocytes expressing either wild type (dieldrin-sensitive) or mutant (dieldrin-resistant) forms of the Drosophila melanogaster GABA-gated chloride channel homo-oligomer, RDL (the product of the resistance to dieldrin locus: Rdl). 2. In the case of the wild type receptor, fipronil blocked GABA-induced currents inducing both a shift to the right in the GABA dose-response curve and depressing the maximum amplitude of responses to GABA. The potency of fipronil was dependent on the GABA concentration but was unaffected by membrane potential. 3. Mutant RDL GABA-receptors, which have a naturally occurring amino acid substitution (A302-->S) in the putative ion-channel lining region, conferring resistance to dieldrin and picrotoxinin, were markedly less sensitive to fipronil than the wild-type receptors. 4. Fipronil antagonism is qualitatively similar to that produced by the structurally distinct compound, picrotoxinin. As the mutation A302-->S reduces the potency of both fipronil and picrotoxinin, homooligomeric RDL receptors should facilitate detailed studies of the molecular basis of convulsant/insecticide antagonist actions on GABA receptors.

Animals↗

PubMed1997

Mortality of workers exposed to dieldrin and aldrin: a retrospective cohort study.

OBJECTIVE: To investigate the occurrence of long term health effects in humans exposed to aldrin and dieldrin, with an update of an earlier retrospective cohort mortality study. METHODS: A group of 570 workers employed between 1 January 1954 and 1 January 1970 either in a production or formulation plant were followed up for mortality until 1 January 1993. There were extensive industrial hygiene data available and biological monitoring data of aldrin and dieldrin for most of the workers. From these data individual estimates were made of the total intake of dieldrin. A total number of 2539.37 person-years at risk was added to the original study. RESULTS: 118 deaths were observed compared with 156 expected. No increase in mortality from liver cancer was found. However, there was an excess in mortality from rectal cancer. This excess was inversely related to the dose gradient. An analysis by job title did not show any excess cancer in any particular job. CONCLUSION: The study does not support a carcinogenic effect of dieldrin and aldrin in humans.

Adult↗